Section 07 · Monograph

Prednisone

Reviewed Nov 2026FDA label

Deltasone / genericCorticosteroid

Indications

Endocrine disorders: primary or secondary adrenocortical insufficiency, congenital adrenal hyperplasia, hypercalcemia associated with cancerFDA-labeled
Rheumatic disorders: rheumatoid arthritis, systemic lupus erythematosus, acute gouty arthritis, psoriatic arthritis, ankylosing spondylitisFDA-labeled
Severe allergic/hypersensitivity conditions: bronchial asthma exacerbations, drug hypersensitivity reactions, serum sicknessFDA-labeled
Dermatologic disease: pemphigus, severe erythema multiforme, exfoliative dermatitis, severe psoriasisFDA-labeled
Ophthalmic inflammatory conditions: uveitis, keratitis, optic neuritisFDA-labeled
Hematologic disorders: autoimmune hemolytic anemia, idiopathic thrombocytopenic purpuraFDA-labeled
Neurologic: acute exacerbations of multiple sclerosis; cerebral edema associated with certain conditionsFDA-labeled

Immunosuppressive therapy for myasthenia gravis, typically as a backbone alongside steroid-sparing agents like azathioprine or mycophenolateOff-label
Other autoimmune/neuroimmunologic conditions: CIDP, autoimmune encephalitis, polymyositis/dermatomyositis, giant cell arteritis/polymyalgia rheumaticaOff-label

Synthetic glucocorticoid that binds the cytoplasmic glucocorticoid receptor; the complex translocates to the nucleus and modulates gene transcription, upregulating anti-inflammatory proteins and downregulating pro-inflammatory cytokines
Inhibits phospholipase A2, reducing prostaglandin/leukotriene production
Broadly suppresses cell-mediated immunity, reducing circulating T-lymphocyte numbers/function and altering antibody production over time
In MG specifically, chronic use is thought to reduce production of pathogenic anti-AChR (or anti-MuSK) antibodies, though the mechanism of the well-documented early paradoxical worsening of MG weakness with steroid initiation is not fully established
Prodrug, hepatically converted to the active metabolite prednisolone

General initial dosage range: 5-60 mg/day orally, individualized to the disease being treated, then titrated to the lowest effective maintenance dose
MG-specific: often initiated at a low dose (e.g., 10-20 mg/day) with slow upward titration, or initiated in a monitored setting, specifically to reduce the risk of transient steroid-induced exacerbation of myasthenic weakness in the first 1-2 weeks
Alternatively, high-dose initiation (e.g., 1 mg/kg/day) may be used under close monitoring, followed by slow taper once improvement is achieved
Long-term MG maintenance commonly targets alternate-day dosing once controlled
Long-term therapy requires gradual tapering rather than abrupt discontinuation to avoid acute adrenal insufficiency
Supplemental ('stress') dosing required during acute illness, surgery, or trauma in patients on chronic therapy

Systemic fungal infections
Known hypersensitivity to prednisone or any component of the formulation
Administration of live or live-attenuated vaccines in patients receiving immunosuppressive doses

CYP3A4 inducers (rifampin, phenytoin, carbamazepine) accelerate metabolism, reducing efficacy
CYP3A4 inhibitors (ketoconazole, certain macrolides) can increase corticosteroid exposure and toxicity
NSAIDs and aspirin increase risk of GI ulceration/bleeding
Concomitant cyclosporine causes mutual inhibition of metabolism, increasing levels/toxicity of both drugs
Live and live-attenuated vaccines should be avoided during immunosuppressive dosing
Potassium-depleting diuretics have additive hypokalemic effect
Hypoglycemic agents/insulin requirements often increase due to steroid-induced hyperglycemia

Hyperglycemia/new-onset or worsened diabetes
Hypertension and fluid/sodium retention, hypokalemia
Increased susceptibility to infections, including reactivation of latent TB or hepatitis B
Osteoporosis, osteonecrosis, myopathy/muscle weakness — clinically important in MG since steroid myopathy can be mistaken for worsening myasthenic weakness
Cushingoid features, weight gain, adrenal suppression with long-term use
Neuropsychiatric effects: mood swings, insomnia, euphoria, depression, rarely psychosis
Posterior subcapsular cataracts, glaucoma
Peptic ulcer disease, GI perforation
Transient worsening of myasthenic symptoms/weakness (including risk of myasthenic crisis) typically within the first 1-2 weeks of initiating or increasing steroid dose

Blood glucose and blood pressure, particularly with new initiation or dose increases
Weight, fluid status, and serum electrolytes (especially potassium)
Bone mineral density (DEXA) with anticipated long-term (>3 months) therapy
Periodic ophthalmologic examination for cataracts/glaucoma with long-term use
Screening for latent infections before starting prolonged immunosuppressive therapy
MG-specific: close clinical monitoring for transient exacerbation of weakness, including respiratory/bulbar function, during the first 2-3 weeks after initiation or dose escalation
Adrenal function assessment when tapering after prolonged therapy

Metabolized by placental 11-beta-hydroxysteroid dehydrogenase to a greater extent than fluorinated steroids, resulting in relatively lower fetal exposure, and is often preferred over fluorinated corticosteroids when maternal treatment is the goal
Chronic maternal use associated with low birth weight and need to monitor neonates for hypoadrenalism
First-trimester exposure has been studied for a possible small increased risk of oral clefts; absolute risk is low
Small amounts excreted into breast milk; low-to-moderate doses generally considered compatible with breastfeeding
Use requires individualized risk-benefit assessment weighing maternal disease control (including MG) against fetal/infant exposure